Post-Ischemic Pathophysiology in the Gerbil Brain — Changes of Extracellular K+ and Ca++

  • T. Yamaguchi
  • H. G. Wagner
  • I. Klatzo
Part of the NATO ASI Series book series (NSSA, volume 115)


It is increasingly recognized that following temporary ischemia cerebral tissue damage may further progress. A protracted development of ischemic injury has been described as “maturation” phenomenon (Ito et al., 1975; Klatzo, 1975). One of its features appears to be the direct relationship between the intensity of the insult and the rate of maturation. A similar relationship has also been observed following recirculation employing biochemical and other parameters (Klatzo, 1975). Irrespective of unequivocal evidence indicating progression of ischemic tissue damage after recirculation, it remains largely obscure which factors are essential and which are merely coincidental. It is also apparent that the selective vulnerability of various brain tissue elements may considerably influence post-ischemic pathology. In order to obtain further insight into the role of the different factors operative in post-ischemic pathophysiology, a model of short-lasting cerebral ischemia was used in which a protracted unfolding of various pathophysiological events could be expected.


Cerebral Ischemia Regional Cerebral Blood Flow Mongolian Gerbil Selective Vulnerability Spontaneous Action Potential 
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  1. 1.
    Diemer NH, and Siemkowicz E, Regional glucose metabolism and nerve cell damage after cerebral ischemia in normo-and hypoglycemic rats, in: “Circulatory and Developmental Aspects of Brain Metabolism”, Spatz M, Mrsulja BB, Rakic L, Lust D, eds., Plenum Press, New York, London (1980).Google Scholar
  2. 2.
    Fujimoto T, Walker JT, Spatz M, and Klatzo I, Pathophysiologic aspects of ischemic edema, in: “Dynamics of Brain Edema”, Pappius H, Feindel W, eds., Springer, Heidelberg, New York (1976).Google Scholar
  3. 3.
    Ginsberg MD, Reivich M, Giandomenico A, and Greenberg JH, Local glucose utilization in acute focal cerebral ischemia: Local dysmetabolism and diaschisis, Neurology 27: 1042 (1977).CrossRefGoogle Scholar
  4. 4.
    Griffiths T, Evans MC, and Meldrum BS, Intracellular sites of early calcium accumulation in the rat hippocampus during status epilepticus, Neurosci Let 30: 329 (1982).CrossRefGoogle Scholar
  5. 5.
    Hass WK, Beyond cerebral blood flow, metabolism and ischemic threshold: Examination of the role of calcium in the initiation of cerebral infarction, in: “Cerebral Vascular Disease”, Meyer JS, Lechner H, Reivich M, Ott EO, Aranibar A, eds., Excerpta Medica, Amsterdam (1981).Google Scholar
  6. 6.
    Hossmann KA, Lechtape-Grüther H, and Hossmann V, The role of cerebral blood flow for the recovery of brain after prolonged ischemia, Z Neurol 204: 281 (1973).CrossRefGoogle Scholar
  7. 7.
    Ito U, Spatz M, Walker JT, and Klatzo I, Experimental cerebral ischemia in Mongolian gerbils. I. Light microscopic observations, Acta Neuropath 32: 209 (1975).CrossRefGoogle Scholar
  8. 8.
    Klatzo I, Pathophysiologic aspects of cerebral ischemia, in: “The Nervous System”, Tower DB, ed., Raven Press, New York (1975).Google Scholar
  9. 9.
    Levy D, Van Uitert R, and Pike C, Delayed post-ischemic hypoperfusion: A potentially damaging consequence of stroke, Neurology 29: 1245 (1979).CrossRefGoogle Scholar
  10. 10.
    Pulsinelli WA, Levy DE, and Duffy TE, Regional cerebral blood flow and glucose metabolism following transient forebrain ischemia, Ann Neurol 11: 499 (1982).CrossRefGoogle Scholar
  11. 11.
    Siesjö BK, Cell damage in the brain: A speculative synthesis, J Cereb Blood Flow Metabol 1: 155 (1981).CrossRefGoogle Scholar
  12. 12.
    Snyder J, Nemoto E, Carroll R and Safar P, Global ischemia in dogs: Intracranial pressure, blood flow and metabolism, Stroke 6: 21 (1975).CrossRefGoogle Scholar
  13. 13.
    Suzuki R, Yamaguchi T, Kirino T, Orzi F, and Klatzo I, The effects of 5-minute ischemia in Mongolian gerbils: I. Blood-brain barrier, cerebral blood flow, and local cerebral glucose utilization changes, Acta Neuropath 60: 207 (1983).CrossRefGoogle Scholar
  14. 14.
    Suzuki R, Yamaguchi T, Li CL, and Klatzo I, The effects of 5-minute ischemia in Mongolian gerbils: II. Changes of spontaneous neuronal activity in cerebral cortex and CA1 sector of hippo-campus, Acta Neuropath 60: 217 (1983a).CrossRefGoogle Scholar
  15. 15.
    Vogt C, and Vogt O, Erkrankungen der Großhirnrinde im Lichte der Topistik, Pathoklise and Pathoarchitektonik, J Psychiatr Neurol 28: 9 (1922).Google Scholar
  16. 16.
    Wagner H, Cahn R, Kuroiwa T, Ting P, Yamaguchi T, and Klatzo I, Role of the blood-brain barrier opening to proteins in pathophysiology of cerebral ischemia, J Cereb Blood Flow Metab 3: S416 (1983).CrossRefGoogle Scholar
  17. 17.
    Walker JL, Specific liquid exchanger microelectrodes, Anal Chem 43: 89A (1971).Google Scholar
  18. 18.
    Welsh FA, Greenberg JH, Jones SC, Ginsberg MD, and Reivich M, Correlation between glucose utilization and metabolite levels during focal ischemia in cat brain, Stroke 11: 79 (1980).CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • T. Yamaguchi
    • 1
  • H. G. Wagner
    • 1
  • I. Klatzo
    • 1
  1. 1.Lab. Neuropath. Neuroanat. Sci.National Institute of Neurological and Communicative Disorders and Stroke National Institutes of HealthBethesdaUSA

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